Blockade of Cav2.2 in inflammatory arthritis leads to up-regulation of the osteoclast activator RANKL (zeige TNFSF11 Proteine) and concomitant joint and bone destruction.

Results identified altered synaptic transmission in the olfactory system of Cav2.2-deficient mice and suggest that the olfactory system could become an attractive model to learn more about this channel and the consequences of its removal

Gaba B receptors were found to mediate Cav2.2 channel inhibition.

Cav2.1 (zeige CACNA1A Proteine)-2.3 have unique contributions to the dynamics at the Schaffer collateral synapse that are engaged by the complex patterns of afferent activity seen in vivo

data suggest that the different roles that Ca(V)2.1 (zeige CACNA1A Proteine) and Ca(V)2.2 play in MNC secretion may be a result of the different levels of expression of Ca(V)2.1 (zeige CACNA1A Proteine) in VP and OT MNCs

CaV2.2 and alpha2delta-1 are intimately associated at the plasma membrane

These findings identify an interaction between ankyrin-B and both Cav2.1 (zeige CACNA1A Proteine) and Cav2.2 at the amino acid level that is necessary for proper Cav2.1 (zeige CACNA1A Proteine) and Cav2.2 targeting in vivo.

CACNA1B Protein Überblick

Protein Überblick

The protein encoded by this gene is the pore-forming subunit of an N-type voltage-dependent calcium channel, which controls neurotransmitter release from neurons. The encoded protein forms a complex with alpha-2, beta, and delta subunits to form the high-voltage activated channel. This channel is sensitive to omega-conotoxin-GVIA and omega-agatoxin-IIIA but insensitive to dihydropyridines. Two transcript variants encoding different isoforms have been found for this gene.